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Neuroscience Week 1 > CNS Neurotransmitters > Flashcards

CNS Neurotransmitters Flashcards

1
Q

small molecule nts

A

aa-glutamate, aspartate, GABA, glycine

  • ach
  • biogenic amines-catecholamines-epi, norepi, dopamine
  • serotonin
  • histamine
  • chemical signals released from pre-synaptic nerve terminals into the synaptic cleft where they can then bind to receptors on postsynaptic cells resulting in a transient change in the electrical properties of the target cell
  • act over tiny distance
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2
Q

peptide nts

A
  • more than 100 different peptides

- 2-36 aa long

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3
Q

nt life cycle

A 
-concentration of nt in cleft controlled via regulation of:
nt synthesis
packaging
release
removal
-removal terminates transmission
-specific for each nt
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4
Q

synthesizing and packaging

A
  • small molecule:
  • synthesized within pre synaptic terminal and packaged into vesicles by specific transport proteins in the vesicle membrane
  • can respond to increased demand rapidly
  • slow axonal transport but fast action
  • neuropeptides:
  • synthesized and packaged into transport vesicles within the cell body, then vesicles down fast
  • cannot respond quickly to increased demand because systhesized in cell body
  • release carefully regulated
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5
Q

ionotropic receptors

A
  • ligand gated ion channels that open in direct response to ligand binding
  • consist of 4 or 5 subunits that each contain 3 or 4 transmembrane domains- have pore loop
  • usually multiple subunits that can be assembled to generate a diverse set of receptors
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6
Q

metabotropic receptors

A

-G protein coupled
activated G proteins modulate ion channels directly or indirectly through intracellular enzymes and second messengers
-monomeric proteins containing 7 transmembrane domains
-wide variety for most nts

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7
Q

ionotropic receptor subunits

A
  • wide variety
  • ampa and nmda are ionotropic
  • 4 or 5 combined to make a functional receptor
  • there are a number of rules that govern which set of subunits are found within each receptors
  • for most each has distinct properties
  • same with metabotropic
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8
Q

amino acid nt

A
  • glutamate

- GABA

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9
Q

biogenic amines

A

-dopa, norepi, serotonin

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10
Q

Ach

A
  • NMJ, synapses in ganglia of visceral motor system
  • in CNS-interneruons in brainstem and forebrain
  • large neurons in the basal forebrain that project to cerebral cortex
  • function in CNS not as well understood-attention, arousal, reward plasticity, enhances sensory functions, damaged associated with memory deficits in AD
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11
Q

Ach in cholinergic nerve terminals

A
  • synthesized in nerve terminal from acetyl coA and choline
  • packaged by vesicular Ach transporter
  • removed from synaptic cleft via cleavage to acetate and choline by AchE
  • choline taken up by nerve terminal via transporter and is used to make more Ach
  • organophosphates and nerve gas can be lethal because they inhibit AchE causing accumulation
  • continued depolarization, muscle paralysis
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12
Q

Ach receptors 1

A
  • nicotinic/ionotropic
  • excitatory cation-selective channels
  • mediate synaptic transmission at NMJ
  • also present in CNS
  • muscle and neuronal receptors have different subunit compositions, both consist of 5 subunits
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13
Q

Ach receptors 2

A
  • metabotropic/muscarinic
  • mediate most Ach in brain
  • highly expressed in forebrain
  • also present in peripheral ganglia where they mediate responses of autonomic effector organs
  • antagonists atropine (pupil dilation) and scopolamine (motion sickness) are therapeutically useful
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14
Q

Myasthenia Gravis

A
  • 14/100,000
  • tired
  • Achreceptor AI disease
  • size of MEPPs reduced, EPPs reduced, probability of post synaptic AP reduced
  • cholinesterase inhibitors, thymectomy, corticosteroids, immunosuppressents
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15
Q

glutamate

A
  • most prominent transmitter for normal brain function
  • nearly all excitatory neurons in brain use it
  • more than half of all brain synapses
  • excitotoxicity
  • high EC concentration toxic
  • excessive activation can excite neuron to death
  • thought to cause neuronal damage during strokes, oxygen deprivation slows glutamate reuptake
  • considerable interest in using glutamate receptor antagonists to block excitotoxic nerve damage following stroke
  • also involved in other acute forms of neuronal insult such as hypoglycemia, trauma, and repeated intense seizures
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16
Q

glutamate in glutamatergic nerve terminals

A
  • glutamate can’t cross blood-brain barrier but glutamine can
  • synthesized in nerve terminal from glutamine
  • can also be synthesized by transamination of alpha-ketoglutarate
  • packaged into vesicles by vesicular glutamate transporter
  • removed from synaptic cleft by high affinity glutamate transporters on both nerve terminal and nearby glial cells
  • in glial cells, glutamate is converted into glutamine and then transported out of the cell and back into nerve terminals
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17
Q

ionotropic glutamate receptors

A
  • ionotropic-NMDA, AMPA, kainate

- excitatory cation selective Na channels

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18
Q

NMDA

A
  • Ca can pass through
  • ion flow is voltage dependent because of Mg 2+ binding
  • glycine binding is required to open channel
19
Q

metabotropic glutamate receptors

A
  • three classes

- activation can increase or decrease excitability of post-synaptic cell

20
Q

GABA and glycine

A
  • major inhibitory nt in CNS
  • GABA is widely distributed in the brain, 1/3 of synapses
  • used by local interneurons in purkinje cells of the cerebellum
  • glycine is predominantly used at synapses in spinal cord
21
Q

GABA in GABAergic nerve terminals

A
  • GABA synthesized in nerve terminals from glutamate, reaction requires pyridoxal phosphate derived from vitamin b6
  • packaged into synaptic vesicles by the vesicular inhibitory amino acid transporter
  • removed from synaptic cleft by specific transporters on nerve ternimals and nearby glia
  • decreased GABA function can cause epilepsy
  • GABA-T turns it into glutamate then glutamine and it becomes like glutamate cycle
22
Q

glycine in glycinergic nerve terminals

A
  • synthesized in nerve terminals from serine
  • packaged by vesicular inhibitory amino acid transporter
  • removed from synaptic cleft by specific transporters on nerve terminals and nearby glia
  • excess glycine caused by defects on glycine transporter causes neonatal disease characterized by lethargy and mental retardation
23
Q

ionotropic GABA and glycine receptors

A
  • GABAa and GABAc
  • inhibitory chloride channels
  • GABA receptor agonists enhance GABAergic transmission
  • benzodazepines-valium
  • barbituates- anesthetics
  • glycine receptor antagonist-strychnine-blocks receptors
  • causes overactivity in spinal cord and brainstem leading to seizures-rat poison
24
Q

metabotropic GABA receptors

A
  • GABAb
  • widely distributed in brain
  • activation produces inhibitory postsynaptic response
25
Q

dopamine, norepi, serotonin

A
  • limited expression of genes for synthesis
  • receptors more broadly expressed
  • compared to GABA and glutamate all over
26
Q

biogenic amines

A
  • aminergic neurons project widely in brain and help modulate intensity of more specific neuronal signals
  • used by relatively few neurons in brain, but very important
  • implicated in wide range of behaviors
  • defects in functions implicated in most psychiatric disorders
  • synthesis in nerve terminals
  • packaged by vesicular monoamine transporter
  • removed by reuptake into nerve terminals
  • receptors are metabotropic, serotonin also has ionotropic
27
Q

catecholamine synthesis

A
  • tyrosine converted to DOPA
  • DOPA converted to dopamine
  • dopamine to norepi
  • norepi to epi
28
Q

sertonin synthesis

A
  • tryptophan converted to 5-hydroxytryptophan

- 5-hydroxytryptophan converted to serotonin

29
Q

distribution of dopamine containing neurons and their projections- substantia nigra

A
  • sends projections to striatum
  • coordination of body movements
  • parkinson’s
  • treated with L-DOPA
  • 80% of brain dopamine found in corpus striatum, which receives major input from substantia nigra
30
Q

midbrain dopamine system

A
  • project from ventral tegmental area to ventral parts of striatium
  • involved in motivation, reward, and reinforcement
  • addictive drugs raise dopamine levels by interfering with reuptake by dopamine transporters
  • minor projections to the cortex involved in emotional behavior
31
Q

projections from locus coeruleus-norepi

A
  • to variety of forebrain and brainstem targets
  • influences sleep and wakefulness, attention, feeding behavior
  • PNS-prominent in sympathetic ganglion cells
  • major transmitter of sympathetic motor system
32
Q

dopamine receptors

A
  • act by activating or inhibiting adenylyl cyclase

- antagonists of receptors in medulla used as anti-emetics to treat nausea and vomiting

33
Q

norepi receptors

A
  • a and b adrenergic receptors
  • agonists and antagonists used therapeutically for many conditions
  • cardiac arrhythmias and migraine headaches
  • most of these effects are mediated by receptors in smooth muscle, not brain
34
Q

catecholamine removal from synaptic cleft

A
  • reuptake into nerve terminals and glia
  • mediated by transmitter-specific plasma membrane transporters
  • cocaine inhibits dopamine transporter causing net increase in release of dopamine
  • amphetamin inhibits both dopamine and norepi transporters causing net increase in release of transmitters
35
Q

serotonin-raphe nuclei in upper brain stem

A
  • project widely to forebrain and brainstem
  • implicated in regulation of sleep, eating, arousal, wakefulness, mood altering
  • drugs used to treat depression-SSRI
36
Q

serotonin

A
  • reuptake into nerve terminal by specific serotonin transporter
  • metabotropic receptors
  • implicated in emotions, circadian rhythms, motor behaviors, mental arousal
  • impairment implicated in many psychiatric disorders
  • activation mediates satiety and decreased food consumption
  • ionotropic receptors-non-selective excitatory cation channel, targets of many drugs including some used to prevent nausea
37
Q

anti-psychotic drugs

A

-block dopamine receptors suggesting excess dopamine release may cause some psychotic illnesses such as schizophrenia

38
Q

anti-anxiety drugs

A
  • MAO inhibitors block breakdown of biogenic amines

- inhibitors of serotonin receptors

39
Q

anti-depressents

A
  • MAO inhibitors block breakdown of biogenic amines
  • tricyclic anti-depressants block reuptake of NE and 5-HT
  • SSRI act specifically on serotonin transporters
40
Q

peptide neurotransmitters

A
  • implicated in modulating emotions, perception of pain, responses to stress
  • biological activity is dependent on the aa seq
  • 5 categories:
  • brain gut
  • opioid
  • pituitary
  • hypothalamic-releasing
  • miscellaneous
41
Q

synthesis and processing of neuropeptides

A
  • synthesized as pre-propeptides in in the ER in neuronal cell body
  • processed into propeptides in ER by removal of ER targeting signal
  • final processing to individual active peptides occurs in vesicles after they bud from trans Golgi
  • individual pro-peptides can give rise to multiple active peptides within a single vesicle
42
Q

peptide neurotransmitters 2

A
  • often co-released with small molecule
  • removed from synaptic cleft via degradation by peptidases
  • some peptides are degraded to more active peptides within the synaptic cleft by endopeptidases
  • use metabotropic receptors-activated at low peptide concentrations and little is known
43
Q

opioid peptides

A
  • widely distributed throughout brain
  • tend to be depressants and can act as analgesics
  • morphine binds to same receptors at opioid peptides

Neuroscience Week 1 (11 decks)

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